Glossary of Block VIII, Week VIII

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general pathophysiology of burn injuries
thermal insult -> vascular damage (release of vasoactive substances)
*subsequent inflammatory rxn, release of inflamm. mediators
*increased vascular permeability, third spacing of fluids
three features seen grossly in burn injury?
1. zone of coagulation (center of injury, non-viable tissue)
2. zone of stasis (marked inflammation, border zone of viability and vascular integrity)
3. zone of hyperemia (viable tissue surrounding injury)
describe 1st - 4th degree burns
1. 1st degree - pain, erythema, reddening of skin surface
2. 2nd - pain, skin blisters
3. 3rd - destruction and ulceration of skin, may be white, leathery, often no pain in center
4. deep injury to SQ tissue
what is the continuum of heat injury?
heat cramps -> heat exhaustion -> heat stroke
medications that predispose to heat injury?
why are antipyretics NOT indicated in heat stroke?
increased temp. is not due to hypothalamic dysfunction
manifestations of heat stroke in:
1. muscles
2. kidneys
3. coagulation ability
4. pulmonary
5. hepatic
1. rhabdomyolysis, elevated CPK
2. insufficiency, acute renal failure
3. DIC, hemorrhage
4. tachypnea, pulmonary edema, ARDS
5. elevated AST, ALT
treatment of heat stroke?
*rapid cooling (ice packs in groin, axillae, neck - NOT on limbs)
4 degrees of frostbite?
1st - edema, erythema, decreased sensation
2nd - clear blister formation
3rd - necrosis of skin, blood filled blisters
4th - skin and soft tissue gangrene
treatment for frostbite?
*rewarming ASAP
*elevation to reduce edema
*protect with sterile dressings, silver sulfadiazine ointment
*oral and topical corticosteroids to decrease release of inflammatory mediators
definition of hypothermia?
body temp <95 deg. F
(body heat loss exceeds production)
mild hypothermia is defined as?
body core T 33-35 deg. C
s/s seen in mild hypothermia?
*cold, shivering
*peripheral vasoconstriction
*lethargy, confusion, impairment of judgement
*decreased fine motor skills
moderate hypothermia is defined as?
body core T 28-32 deg. C
s/s of moderate hypothermia?
*increasing CNS depression, stupor
*cardiorespiratory depression (hypotension, bradycardia, bradypnea)
*peripheral vasoconstriction
*risk of atrial & ventricular arrythmias
severe hypothermia is defined as?
core body T <29 deg.C
s/s of severe hypothermia?
*loss of thermoregulatory control
*unresponsive, fixed pupils
treatment of hypothermia?
rapid rewarming
bretylium for arrythmias
describe the ECG changes seen in severe hypothermia
Osborne waves (J waves)
what is the difference between an:
1. exogenous infection
2. endogenous infection
3. toxin-induced skin disease
1. MC - cuts, bites, skin disease, burns
2. skin manifestations of an underlying disease process. (systemic infections, underlying tissue)
3. toxin produced at a different site
what are some environmental factors that increase the chance of exogenous infection?
introduction of foreign body
pressure (ie. bedsore)
compromised blood supply (PVD, DM)
what is folliculitis?
infection of hair follicles
where on the body is folliculitis MC seen?
areas of friction and sweat gland activity
MCC of folliculitis?
Staph aureus
which bacteria causes "hot-tub" folliculitis?
P. aeruginosa
which bacteria is a major skin anaerobe that contributes to acne?
Propionibacterium acnes
what is furuncle?
BOIL - small abscess in the region of a hair follicle
MCC of furuncles?
Staph aureus
what leads to recurrent furunculosis?
repeated self-inoculation
a confluence of multiple furuncles becomes a ?
treatment for furuncles and folliculitis
most are self-resolving
(furuncles may require drainage)
treatment for chronic furunculitis?
bacitracin, neomycin cream
treatment for carbuncles?
surgical drainage, Abx. tx (cloxacillin, flucloxacillin)
what class of exogenous infections do the following belong to: impetigo, erysipelas, cellulitis?
spreading infections
four exotoxins of Staph aureus?
1. alpha toxin
2. exfoliatin
3. PTSAgs (pyrogenic toxin superantigens)
4. TSST-1 (toxic shock syndrome toxin)
which exotoxin is found in almost all S. aureus?
alpha toxin
function of alpha toxin of S. aureus?
forms pores in lipid bilayer
(causing cell lysis, death, tissue necrosis)
function of exfoliatin toxin of S. aureus?
cleaves desmoglien, separates skin layers
which Staph exotoxin is produced by a bacteriophage?
two exotoxins found in Streptococcus pyogenes?
M protein
SPEs (streptococcal pyrogenic antigens)
which strep exotoxin is present on all strep?
M protein (surface protein)
significance of M protein as an exotoxin for strep?
can determine the sequelae fo a strep infection (ie. nephrotogenicity)
how many different SPE toxins are there?
SPE types A and B are associated with?
toxic shock
SPE type C is associated with?
scarlet fever
what is the difference between impetigo, erysipelas, and cellulitis?
impetigo - confined to epidermis
erysipelas - involved dermal lymphatics
cellulitis - major focus is SQ fat layer
in general, which is the more aggressively spreading bacteria when it comes to skin infections: staph or strep?
(opposite of endocarditis)
two MC organisms found in impetigo?
what is the characteristic clinical appearance of impetigo?
honey colored crust
in impetigo - what is significant about the exudates and crust?
contain infectious bacteria (if the crust is not removed, new lesions form about the periphery)
possible complication of impetigo caused by group A strep?
poststreptococcal glomerulonephritis
treatment of impetigo?
bacitracin or mupirocin to limit spread
(treatment may not prevent glomerulonephritis)
strains of S. aureus with the group II bacteriophage may cause what skin infection?
bullous impetigo
function of group II bacteriophage in S. aureus?
encodes for exfoliatin toxin (this cleaves desmoglein in epidermis, results in superficial flaccid bullae that are easily ruptured)
treatment for bullous impetigo?
anti-staph antibodies
MCC of erysipelas?
(pyogenes, occasionally group B, C or D)
erysipelas are MC in which age group?
describe an erysipela
abrupt onset
fiery red swelling of face or extremities
well defined margins
rapid progression
intense pain
erysipelas can progress to?
local skin necrosis
treatment for erysipelas?
describe the borders of cellulitis compared to the borders of erysipelas
cellulitis - borders blend with surrounding tissues
erysipelas - distinct borders
describe the clinical presentation of cellulitis
localized pain
can spread rapidly
what may cellulitis be accompanied by?
lymphangitis and inflammation of draining lymph nodes
two MCC of cellulitis?
Staph aureus
Strep pyogenes
which is worse - staph or strep cellulitis?
(more rapidly spreading, diffuse, frequently associated with lymphangitis and fever)
recurrent strep cellulitis is due to what strains?
group A, C or G strep PLUS skin lesions
when is recurrent staph cellulitis seen?
in immunocompromised or chronic nasal carriers
what bacteria commonly causes cellulitis in DM and PCD?
Strep agalactiae
what bacteria commonly causes periorbital cellulitis in children?
Haemophilus influenza type b
(spread from sinusitis, otitis media, epiglottitis)
what bacteria, commonly found in aquatiums, causes cellulitis?
Mycobacterium marinarum
when is pseudomonas cellulitis MC seen?
hospitalized and immunocompromised hosts
treatment of cellulitis?
MC wound pathogen in clean surgical wounds?
Staph aureus
pathogen found in cat bite wounds?
Pasteurella multocida
MC pathogen in burn wounds?
Pseudomonas aerunginosa
MC pathogen in puncture wounds?
Clostridium tetani
MC pathogen in traumatic wounds?
Clostridium perfringens
describe the shape and gram staining of Pasteurella multocida
gram negative rod
what is characteristic about the staining of Pasteurella multoceda?
bipolar staining
biochemical characteristics of Multocida pasteurella?
catalase +
oxidase +
facultative anaerobe
where is Pasteurella multocida commonly found?
normal flora in respiratory and GI tracts of animals and birds
two virulence factors posessed by Pasteurella multoceda?
capsule (antiphagocytic)
complications of a Pasteurella multoceda infection?
*septicemia, meningitis
treatment for a Pasteurella multoceda infection?
penicillin or tetracycline
*unless* cat bite -> then treat with ampicillin and don't suture!
25% of burns result in?
pseudomonal infection
(can lead to septicemia with >50% mortality)
regarding pseudomonas:
1. gram stain, structure
2. oxidase
3. fermenting or non-fermenting?
4. aerobe or anaerobe?
1. gram - rod
2. oxidase +
3. non-fermenting
4. primarily aerobe
what is significant about the nutrient requirements of Pseudomonas aeruginosa?
not many nutrients required, can grow in distilled water and many other environments
significance of the water soluble pigments produced by pseudomonas?
*can flouresce under UV light
*green pus typical
*fruity odor
function of the following virulence factors posessed by pseudomonas?
1. pili
2. flagella
3. capsule
1. attachment
2. dissemination
3. antiphagocytic
function of the following exotoxins produced by pseudomonas aeruginosa?
1. elastase
2. alkaline phosphatase
3. phopholipase C
4. heat stabile phospholipase
1. tissue damage
2. proteolysis, tissue damage
3. tissue damage
4. tissue damage
treatment of burns infected with pseudomonas aeruginosa?
*topical application of antibacterial agents (ie. silver nitrate)
*surgical debridement
best antibiotic combination to treat pseudomonas?
-aminoglycoside + extended spectrum penicillin
describe clostridium in the following context:
1. gram stain, shape
2. aerobe or anaerobe
3. spore or no spore?
1. gram + rod
2. strict anaerobe
3. spore forming
MC species in clostridium cellulitis?
C. perfringens
what causes the crepitus felt in clostridial cellulitis?
gas found in skin
treatment of clostridial cellulitis?
what is the difference between type I and II necrotizing fasciitis?
type I - seen in pts following a surgical procedure, with DM or severe PVD (caused by mixed aerobic and anaerobic bacteria)
type II - formerly streptococcal gangrene, caused by group A strep.
bacterial causes of synergistic necrotizing fasciitis?
combination of gram - rods and strict anaerobes (ie. Bacteroides or Clostridia)
where is necrotizing fasciitis commonly seen?
on or about feet
(rapid extension along fascia in to leg)
treatment for necrotizing fasciitis type I?
ampicillin PLUS clindamycin PLUS FQ
four types of "endogenous" skin infections?
noninfectious lesion
MCC of abscesses?
intravascular infx (esp. staph aureus)
two manifestations of necrosis?
purpura fulminans
ecthyma gangrenosum
what is purpura fulminans?
skin manifestations of DIC
when is erythmea gangrenosusm commonly seen?
in immunocompromised
usually with P. aeruginosa
what type of rash would be seen in meningiococcemia?
hemorrhagic rash
what type of rash is seen in typhoid fever, rocky mountain spotted fever?
macular rash
scarlet fever is caused by?
group A strep exotoxin
scalded skin syndrome and TSS are caused by what bacteria?
SSSS is most commonly seen in which age group?
children <5yr (including neonates)
SSSS is caused by what in particular?
Staph aureus group II
*toxin - exfoliatin
TSS is caused by what in particular?
toxic shock sydrome toxin (TSST) - present in 5-25% of S. aureus
can Strep cause a toxic shock syndrome?
strep can produce pyrogenic exotoxins that cause streptococcal toxic shock syndrome (STSS)
skin manifestations of TSS?
diffuse red rash
*lasts 1-2 wks, then see peeling of skin
other clinical s/s of TSS?
*redness of eyes, mouth, throat
*confusion, seizures, H/A
*organ failure
mortality rate of TSS?
treatment of TSS?
fluid replacement
general supportive care
gamma globulin
1. autograft
2. syngeneic graft
1. from one part of an individual to another part of the same individual
2. between genetically identical individuals of the same species
1. allogeneic graft (allograft)
2. xenogeneic graft (xenograft)
1. between genetically disparate individuals of the same species
2. between individuals of different species
most grafts are of what type?
what are the two ways in which recipient T cells can be activated against graft antigens?
1. direct recognition (some transplants)
2. indirect recognition (all transplants)
describe indirect recognition of graft antigens
host APCs activate host T cells using host MHC molecules
describe direct recognition of graft antigens
donor APCs activate host T cells in host lymph node using donor MHC molecules
(donor MUST have same MHC molecules as host in order for this to occur)
compate the rejection time of a primary allograft vs a secondary (repeated) allograft
primary - longer time to rejection
secondary - shorter time until rejection due to immunological memory
initial graft rejections are usually due to what immune response?
T cell activity
(NOT antibodies)
in relation to major and minor histocompatibility genes, discuss the:
major - MHC I and II
minor - all chromosomes
in relation to major and minor histocompatibility genes, discuss the:
# of loci
major: 5-10
minor: 100+
in relation to major and minor histocompatibility genes, discuss the:
rejection speed
major - rapid
minor - variable
in relation to major and minor histocompatibility genes, discuss the:
generation of Ab
major - lots of Ab generated
minor - few if any made
in relation to major and minor histocompatibility genes, discuss the:
major - high (lots of variety)
minor - low
in relation to major and minor histocompatibility genes, discuss the:
major - Ag presentation
minor - ?
in relation to major and minor histocompatibility genes, discuss the: tolerization by the host immune system
major - difficult
minor - easier
what is the "law of transplantation"
a recipient MAY reject a graft if that graft expresses histocompatibility genes (antigens) not
expressed by host genes
[recipient may reject a graft if it is foreign]
what happens to a graft that is taken from a homozygote and given to a heterozygote?
what heppens to a graft that is taken from a heterozygote and goven to a homozygote?
what are the 3 patterns of rejection?
1. chronic rejection
2. acute rejection
3. hyperacute rejection
T cells mediate what kinds of rejection?
chronic and acute rejection
how long for graft destruction in chronic rejection?
weeks -> months -> years
how long for graft destruction in acute rejection?
10-14 days
what is the hyperacute rejection mediated by?
(Abs are usually against MHC class I)
two situations in which hyperacute rejection occurs?
1. recipient is repeatedly exposed to graft antigens
2. naturally occuring Ab exists
how fast is the graft destroyed in a hyperacute rejection?
within a few days
why is there little cellular infiltrate seen in a hyperacute rejection compared to the other rejection types?
no time for vasculature to get established - therefore no way for inflammatory cells to get there
(other graft types have time for vasculature to get established)
incompatibilities with minor histocompatiblity genes generally results in what type of rejection?
incompatibilities with major histocompatiblity genes generally results in what type of rejection?
which type of organ transplant is hyperacute rejection commonly seen in?
what are some factors affecting graft rejection?
1. presensitixation
2. degree of genetic mismatch
3. lymphatic drainage
4. tissue typ einvolved
5. graft size
6. immune response genes
describe lymphatic drainage issues in relation to graft rejection
decrease lymphatic drainage, increase chance of survival (less way for APCs and T cells to drain to lymph nodes)
describe graft size in relation for graft rejection
increased graft size sometimes increases survivability "overwhelmed immune system"
what is significant about liver transplants and rejection?
liver transplants seen to be viable across genetic barriers (HLA mismatch)
(many surgeons believe that HLA matching has no relevance to survival of liver transplants)
what is a unique type of rejection seen in bone marrow transplants?
graft-vs-host (GVH)
how can acute GVH be prevented?
deplete marrow of mature T cells before transplanting
does MHC matching need to be performed for bone marrow transplants?
yes - some needs to be done
(necessary for positive and negative selection to operate)
why do T cells not respond well to xenografts?
MHC I and II molecules on those cells re too different to fil well with host TCRs
3 mechanisms of hyperacute rejection seen in xenografts?
1. pre-existing antibodies to carbohydrate structures
2. compliment
3. MK cell mediated killing of donor cells lacking appropriate MHC I molecules
what happens when pig cells are transfected with human DAF, CD59 genes, etc?
pig cells are now able to INACTIVATE HUMAN COMPLIMENT components binding to their surface
what happens when pig cells are transfected with human MHC I genes?
pig cells now have MHC I molecules to bind inhibitory receptors on human NK cells and prevent attack
how can a general immune deficiency be induced in order to minimize/prevent reaction to a graft?
1. radiation
2. Ab against T cell markers
3. drugs cytotoxic for rapidly dividing cells
4. drugs with narrow specificity for proliferating T cells (cyclosporin)
Cutaneous manifestations of:
1. papillomavirus
2. parvovirus B19
3. herpesviruses - HSV and VZV
4. herpesviruses - EBV and HHV-6
5. herpesviruses - CMV
6. smallpox
1. papules
2. macules, papules
3. vesicles
4. macules
5. macules, papules
6. vesicles, pustules
cutaneous manifestations of
1. coxsackie
2. measles
3. rubella
1. vesicles
2. macules, papules
3. macules
following the primary infection - where does VZV establish latent infection?
dorsal root ganglia
extramedullary cranial nerve ganglia
in what type of patients does VZV cause serious morbidity and mortality?
immunosuppressed patients
recurrent VZV disease is called?
Zoster or shingles
most cases of VZV occur in what population?
children <15yrs
seasonality to VZV?
winter and early spring
incidence of Zoster in pts that have had varicella?
reactivation of VZV is associated with what conditions?
seasonality for zoster?
manifestations of zoster in the immunocompromised?
may disseminate
(causing skin lesions, CNS, pulmonary, hepatic involvement)
transmission of VZV?
Aerosolized droplets
Direct contact
*very contagious*
describe the pathogenesis of a primary VZV infection
* virus spreads to lymphatics, then to blood
*viremia causes seeding of liver and spleen
*secondary viremia occurs about 14 days post infection - manifests as infection of skin and mucosal surfaces
describe Ig levels after a VZV infection
IgM and IgA decrease after 1yr
IgG declines but persists at a low level
what type of immunity plays a role in host defense against recurrent VZV infection?
cellular immunity
NK cells
paitents that are deficient in cell mediated immunity are at risk of?
severe disease caused by VZV
incubation period of VZV?
14-17 days
(shorter in immunocompromised pts)
in which patient group are prodromal symptoms of VZV absent?
young children
prodromal symptoms seen in older pts?
fever (1-6 days)
sore throat
describe the appearance and character of the varicella rash
crops of vesicles appear every 2-4 days
*rash appears on trunk first, then spreads to limbs
in what stage of the rash is moderate to severe pruritis present?
vesicular stage
evolution of the vesicles in a chickenpox rash
1. thin walled vessicle with clear fluid ->
2. vesicle becomes cloudy and depressed in center with irregular border ->
3. crust forms in center and eventually replaces remaining portion of vesicle at periphery
when is the vesicle no longer infectious?
when it crusts
describe the skin lesions seen in shingles
*crops of varicella like lesions
*involves a single dermatome
*pain, parasthesias
*never cross midline
MC reactivation of VZV occurs at which spinal levels?
trunk (T3-L2)
DDx of zoster that involves trigeminal nerve?
MC complication of VZV in children?
bacterial infection
other complications of VZV?
when is hemorrhagic chickenpox seen?
immunocompromised pts
(50% mortality rate)
a bacterial infection of chickenpox can result in?
bullous impetigo
treatment of VZv if needed?
what type of VZV vaccine is available?
live, attenuated
(doesn't prevent shingles)
what can be given to provide passive immunization to chickenpox?
(varicella zoster immunoglobulin)
*effective when administered up to 3 days after exposure
major use for VZIG?
immunocompromised children
newborn infants whose mothers have active varicella at the time of delivery
HHV-6 causes what childhood disease?
roseola infantum (exanthema subitum - "sudden rash")
characterize the onset of roseola infantum?
fever as high as 105
lasts 3-4 days
in roseola infantum - what occurs after the rash?
(fever is prodromal)
where does HHV-6 primarily infect and replicate?
CD4+ T cells
describe the rash and prognosis of roseola infantum (exanthema subitum)
faint macular rash
mild self-limiting disease
hand-foot-and mout disease (HFMD) is primarily caused by?
coxsackie viruses A9, A16
enterovirus 71
what is the classic sign of HFMD?
exanthema on buccal mucosa
(also found on dorsum of hands and margin of heels)
HFMD primarily occurs in which population?
children <4 yrs of age
herpangina is primarily caused by?
coxsackie A viruses
describe the s/s of herpangina
abrupt onset
fever, sore throat, excessive salivation
*grouped, grey vesicles in mouth
course of herpangina?
*self limiting*
fever lasts 1-4 days
disease lasts 4-5 days
how many serotypes of measles are there?
(reason for effectiveness of vaccine)
function of H and F protien located on viral envleope of the measles virus?
H protien - promotes attachment to cell receptors
F protien - promotes viral-cell and cell-cell fusion
transmission of measles?
respiratory droplets
direct contact with nasal or throat secretions
how long after the rash appears is transmission of measles possible?
4-5 days
what is a characteristic histologic feature of measles infection?
multinucleated giant cells
(with eosinophilic and intranuclear inclusion bodies)
how does measles cause immunosuppression?
*infects lymphocytes, monocytes, macrophages
*inhibits lymphocyte proliferation
how long can clinically significant immunosuppression last post-infection?
up to 1 yr
how long do antibodies to measles persist?
for life
what immune response is responsible for most symptoms seen in measles?
cellular immune response
how does measles differ in a CMI deficient patient?
no rash
describe the prodromal phase of measles. when does it begin?
*low grade fever, malaise
*coryza, sore throat, H/A
*sneezing and cough
begins 8-12 days after infection
what are Koplicks spots and when do they appear in relation to the measles rash?
red patches with central white specks that appear on buccal mucosa 2-3 days prior to onset of measles rash
describe the rash seen in measles. where does it begin and spread?
begins at hairline - rapidly progresses to the face, neck trunck and extremities
complications fo a measles infection?
inner ear infx
acute postinfectious encephalitis
death in a measles infection in children <2yrs is MC due to what complication?
treatment for measles?
(no antivirals)
what type of vaccine is the measles?
live, attenuated
measles vaccine is contraindicated in?
allergy to eggs, neomycin
comprised immunity
what is unique about the replication of the smallpox virus?
replicates entirely in the cytoplasm of the cell
(large dsDNA genome, doesn't need nucleus to replicate)
transmission of smallpox?
respiratory route
what is characteristic about the smallpox lesions?
*all lesions are in the same stage of development
*centrifugal (distal) rash distribution
*lesions on palms and soles
(firm, round, deep seated pustules)
describe the prodrome seen in smallpox
fever >101
prostration, H/A, backache, chills, vomiting, abd. pain
where do the first lesions in smallpox appear?
oral mucosa, face or forearms
the other diseases caused by poxviruses?
1. molluscum contagiosum
2. ORF
3. cowpox
what is the signifance of cowpox in relation to smallpox?
provides immunity to smallpox
does pseudocowpox provide immunity to smallpox?
most vaccine responses are due to which immune response (innate or adaptive)
(specificity, memory)
what are the three pathogen repication sites in the body (therefore the 3 points of focus for the immune response)?
1. vesicular
2. cystosolic
3. extracellular
where do most pathogenic bacteria replicate?
where do most viruses live?
which type of immune response activates macrophages to kill intravesicular pathogens?
Th1 response
whic type if immune response activates B cells to make antibodies and occurs extracellularly?
influenza vaccine has been "associated with"?
Guillan Barre syndrome
HBV vaccine has been "associated with"
MMR vaccine has been "associated with"
aluminum containing vaccines have been "associated with"?
(macrophagic myofaciitis)
what is a first generation vaccine?
live or attenuated
dead or inactivated
what is a second generation vaccine?
extracts (proteins, peptides)
what is a third generation vaccine?
(currently in clinical trials)
2 risks of an attenuated vaccine?
1. necessary epitopes not present
2. wild-type reversion
give an example of a dead or inactivated vaccine
give an example of an extract vaccine
diptheria and tetanus toxins
give an example of a conjugated vaccine
(direceted against Haemophilus protein, LPS protein used for immunogenesis)
what is a conjugated vaccine?
desired pathogenic epitope is combined with an immune stimulatory molecule (ie. LPS)
DNA vaccines are currently experimental for?
how is an adjuvant useful in enhancing the efficacy of a vaccine?
enhances the immunogenicity by acting on APCs
risks of using an adjuvant in a vaccine?
induction of inflammatory diseases (SLE, MS)

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